| pubmed-article:10861013 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10861013 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
| pubmed-article:10861013 | lifeskim:mentions | umls-concept:C0003241 | lld:lifeskim |
| pubmed-article:10861013 | lifeskim:mentions | umls-concept:C0332461 | lld:lifeskim |
| pubmed-article:10861013 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
| pubmed-article:10861013 | lifeskim:mentions | umls-concept:C0205360 | lld:lifeskim |
| pubmed-article:10861013 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:10861013 | lifeskim:mentions | umls-concept:C0205421 | lld:lifeskim |
| pubmed-article:10861013 | pubmed:issue | 13 | lld:pubmed |
| pubmed-article:10861013 | pubmed:dateCreated | 2000-7-31 | lld:pubmed |
| pubmed-article:10861013 | pubmed:abstractText | In the present study, we investigated the role of the CD40L-CD40 pathway in a model of progressive atherosclerosis. ApoE-/- mice were treated with an anti-CD40L antibody or a control antibody for 12 wk. Antibody treatment started early (age 5 wk) or was delayed until after the establishment of atherosclerosis (age 17 wk). In both the early and delayed treatment groups, anti-CD40L antibody did not decrease plaque area or inhibit lesion initiation or age-related increase in lesion area. The morphology of initial lesions was not affected, except for a decrease in T-lymphocyte content. Effects of anti-CD40L antibody treatment on the morphology of advanced lesions were pronounced. In both the early and delayed treatment groups, T-lymphocyte content was significantly decreased. Furthermore, a pronounced increase in collagen content, vascular smooth muscle cell/myofibroblast content, and fibrous cap thickness was observed. In the delayed treatment group, a decrease in lipid core and macrophage content occurred. Interestingly, advanced lesions of anti-CD40L antibody-treated mice exhibited an increased transforming growth factor beta1 immunoreactivity, especially in macrophages. In conclusion, both early and delayed treatment with an anti-CD40L antibody do not affect atherosclerotic lesion initiation but do result in the development of a lipid-poor collagen-rich stable plaque phenotype. Furthermore, delayed treatment with anti-CD40L antibody can transform the lesion profile from a lipid-rich to a lipid-poor collagen-rich phenotype. Postulated mechanisms of this effect on plaque phenotype are the down-regulation of proinflammatory pathways and up-regulation of collagen-promoting factors like transforming growth factor beta. | lld:pubmed |
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| pubmed-article:10861013 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10861013 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10861013 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10861013 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:10861013 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:10861013 | pubmed:author | pubmed-author:KotelianskyV... | lld:pubmed |
| pubmed-article:10861013 | pubmed:author | pubmed-author:DaemenM JMJ | lld:pubmed |
| pubmed-article:10861013 | pubmed:author | pubmed-author:BurklyL CLC | lld:pubmed |
| pubmed-article:10861013 | pubmed:author | pubmed-author:HeenemanSS | lld:pubmed |
| pubmed-article:10861013 | pubmed:author | pubmed-author:CleutjensK... | lld:pubmed |
| pubmed-article:10861013 | pubmed:author | pubmed-author:LutgensEE | lld:pubmed |
| pubmed-article:10861013 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10861013 | pubmed:day | 20 | lld:pubmed |
| pubmed-article:10861013 | pubmed:volume | 97 | lld:pubmed |
| pubmed-article:10861013 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10861013 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10861013 | pubmed:pagination | 7464-9 | lld:pubmed |
| pubmed-article:10861013 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10861013 | pubmed:meshHeading | pubmed-meshheading:10861013... | lld:pubmed |
| pubmed-article:10861013 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10861013 | pubmed:articleTitle | Both early and delayed anti-CD40L antibody treatment induces a stable plaque phenotype. | lld:pubmed |
| pubmed-article:10861013 | pubmed:affiliation | Department of Pathology, Cardiovascular Research Institute Maastricht, University of Maastricht, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands. | lld:pubmed |
| pubmed-article:10861013 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10861013 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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